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Physiology · Systemic architectonics of behavioral acts

Experimental neuroses

Experimental neuroses are artificially induced pathological states of higher nervous activity. They are characterized by a profound breakdown of nervous processes, the disappearance of previously established conditioned reflexes, and the onset of pronounced somatic disorders.

Discovery of the phenomenonFormulated by I.P. Pavlov in 1924 following the flood in Petrograd.
Vulnerable typesWeak type ("melancholics") and strong unbalanced type ("cholerics").
HNA symptomViolation of the law of strength and the development of phase states.
Trophic shiftsDull coat, hair loss, formation of trophic ulcers.
3 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

History and core of the problem

The study of the pathology of higher nervous activity began due to an accidental incident. During the catastrophic flood in Petrograd in 1924, laboratory animals at I.P. Pavlov's institute were subjected to extreme emotional stress. Upon rescue, researchers discovered that the dogs had developed a severe neurotic state. The main manifestation of this disorder was the complete disappearance of all conditioned reflexes that had been painstakingly developed over months prior to the incident. This case became the starting point for targeted experimental modeling of nervous activity breakdowns.

Etiology and pathogenesis of higher nervous activity breakdowns

To induce a neurotic state in laboratory conditions, researchers use specific techniques aimed at depleting the nervous system's resources. Four main pathways for neurosis formation are distinguished:

  1. Overstrain of the excitatory process. It occurs when the animal is presented with extremely strong conditioned stimuli. As a result, a breakdown occurs, and protective inhibition begins to prevail in the cerebral cortex. Clinically, this manifests as drowsiness and the extinction of reflexes. Animals with a weak constitution ("melancholics") fall into the risk group.
  2. Overstrain of the inhibitory process. It develops when the animal is required to perform overly fine differentiations (distinguishing very similar stimuli) or when the time between the conditioned signal and reinforcement is excessively prolonged. A breakdown toward pathological excitation occurs: inter-signal responses and continuous salivation appear. Animals of the strong unbalanced type ("cholerics") are most vulnerable to this mechanism.
  3. "Clashing" ("sshishka") of nervous processes. A special term introduced by I.P. Pavlov. It denotes a pathogenic situation in which there is a sharp, almost instantaneous transition from the excitatory process to the inhibitory one or vice versa.
  4. Disruption of the dynamic stereotype. A deep neurotic state is triggered by a sudden and drastic breakdown of the habitual system of behavioral reactions.
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Clinical presentation and phase phenomena

Experimental neuroses are not limited to the mere loss of reflexes. This is a systemic disorder that affects the entire organism. Characteristic signs are divided into three groups:

1. Violation of the law of strength Normally, a strong stimulus elicits a strong response, and a weak one elicits a weak response. In neurosis, pathological phase phenomena develop:

  • Equalization phase: reflex responses to strong and weak stimuli become absolutely identical.
  • Paradoxical phase: a perversion of reactions occurs. Positive signals begin to induce inhibition, while inhibitory stimuli provoke a positive conditioned reflex response.
  • Inhibitory phase: complete areflexia (disappearance of all responses) sets in.

2. Behavioral changes The animal actively resists being brought into the experimental room. Inappropriate motor activity, constant vocalization (howling, whining), and a sharp increase in the number of restless inter-signal responses are observed.

3. Autonomic symptoms A nervous breakdown inevitably hits somatic health. In the cardiovascular system, elevated blood pressure, extrasystoles, and shortness of breath are recorded. The skin integument suffers: the coat becomes dull and falls out, and long-healing trophic ulcers may appear. Often, these changes are functional in nature and regress after the cessation of the stressor. However, in severe breakdowns, special pharmacological treatment is required to restore functions.

How to memorize

To remember the sequence of phases in neurosis (from mild to severe), the Russian acronym UPT can help: Equalization (Uravnitelnaya) → Paradoxical (Paradoksalnaya) → Inhibitory (Tormoznaya).

Class and exam questions

This is one of the mechanisms of neurosis development, in which there is a rapid and sharp transition from the excitatory process to the inhibitory one or vice versa.

This is one of the mechanisms of neurosis development, in which there is a rapid and sharp transition from the excitatory process to the inhibitory one or vice versa.

Which animals are prone to a breakdown toward inhibition?

A breakdown with a predominance of inhibition is characteristic of animals with a weak type of higher nervous activity ("melancholics") during the overstrain of the excitatory process.

What happens in the paradoxical phase?

In this phase, the law of strength is perverted: positive conditioned signals cause an inhibitory response, and a reflex response occurs to inhibitory stimuli.

Do experimental neuroses need to be treated pharmacologically?

In most cases, autonomic and behavioral disorders resolve on their own after the removal of the neurotizing factor. But in severe cases, pharmacological intervention is required.

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What else to study on this topic

  • The law of strength in normal physiology
  • Classification of higher nervous activity types according to I.P. Pavlov (cholerics, sanguines, phlegmatics, melancholics)
  • Mechanisms of formation and destruction of the dynamic stereotype
  • Pathophysiology of autonomic disorders in stress
  • The nature of neurogenic trophic ulcers

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